A novel method for analysis of human T cell repertoires by real-time PCR.

T lymphocyte responses to challenges with multiple pathogens depend on the diversity of their T cell receptors (TcRs) that are heteroduplexes of alpha and beta chains. The regions of alpha and beta chains that define TcR specificity are encoded by rearranged variable (V) and joining (J) genes that are separated by variable numbers of nucleotides that encode the complementarity determining region 3 (CDR3). The assumption that a "healthy" T cell compartment exhibits broad TcR and CDR3 diversity has driven development of methods to evaluate diversity of TcR beta transcripts expressed by T lymphocyte populations and subpopulations in inflammatory sites and human malignancies.

MHC class II epitope nesting modulates dendritic cell function and improves generation of antigen-specific CD4 helper T cells.

CD4 Th cells are critical to the development of coordinated immune responses to infections and tumors. Th cells are activated through interactions of the TCR with MHC class II complexed with peptide. T cell activation is dependent on the density of MHC peptide complexes as well as the duration of interaction of the TCR with APCs.

Distributions of single nucleotide polymorphisms in differential chromosome segments of congenic resistant strains that define minor histocompatibility antigens.

Minor histocompatibility antigens (MiHAs) stimulate the rejection of allografts when donors and recipients are matched at the major histocompatibility complex (MHC). The majority of identified autosomal MiHAs were generated by non-synonymous (NS) substitutions that alter MHC class I-binding peptides. The mosaic distribution of single nucleotide polymorphisms (SNPs) that distinguish inbred mouse strains led us to hypothesize that MiHA genes defined by congenic strains on C57BL/6 and C57BL/10 backgrounds map to chromosomal regions with relatively high numbers of NS SNPs that distinguish C57 strains from other common inbred strains.

Expression of mRNA for a newly identified Pax5 exon is reduced in multiple myeloma.

Pax5 is a transcription factor that is critical in the bone marrow for differentiation and proliferation of B cells until the plasma cell stage. In Pax5(-/-) mice, B-cell development stalls at the pro-B-cell stage. Messenger RNA profiles of alternatively spliced isoforms of Pax5 in bone marrow frequently differ between multiple myeloma (MM) patients and healthy donors.

Cysteine-tailed class I-binding peptides bind to CpG adjuvant and enhance primary CTL responses.

Immunostimulatory CpG motifs in synthetic oligonucleotides can be effective adjuvants for the priming of CTLs. We first observed that a single male-specific peptide (KCSRNRQYL) (HY2) was more efficient than another male-specific peptide (WMHHNMDLI) (HY1) at priming IFN-gamma-secreting CTLs in vivo when combined with lipid A and CpG and that it also visibly precipitated CpG. The addition of the six N-terminal residues (KCSRNR) from HY2 to HY1 yielded a peptide, KCSRNR-HY1, that both precipitated CpG and primed increased numbers of HY1-specific CTLs.

Mitosis increases levels of secretory leukocyte protease inhibitor in keratinocytes.

Chronic wounds are a major health care burden. Multiple factors produced by healing wounds play important roles in efficient and orderly wound healing. Secretory leukocyte protease inhibitor (SLPI) is constitutively expressed in epithelial cells, and its expression is increased by inflammation.

Altered mRNA expression of Pax5 and Blimp-1 in B cells in multiple myeloma.

Multiple myeloma (MM) is a plasma cell disorder that potentially initiates during an early stage of B-cell development. We encountered an unidentified isoform of B cell-specific activator protein (BSAP, or Pax5) in MM cells while performing differential analyses to compare mRNA expression in malignant and normal plasma cells. Pax5 is a transcription factor that plays a central role throughout B-cell development until the point of terminal differentiation.